SmarcAL1 Antibody [K9N14] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:100-1:1000 IP1:100-1:200 IHC1:50-1:500 IF1:50-1:500

Application
WB, IP, IHC, IF, ELISA

Reactivity
Human, Mouse, Rat

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
106 kDa 110 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
SmarcAL1 Antibody [K9N14] detects endogenous levels of total SmarcAL1 protein.

Clone
K9N14

Synonym(s)
SNF2 related chromatin remodeling annealing helicase 1, Sucrose nonfermenting protein 2-like 1, SMARCAL1, HARP

Background
SMARCAL1 (SWI/SNF‑related, matrix‑associated, actin‑dependent regulator of chromatin subfamily A‑like 1) is an ATP‑dependent annealing helicase of the SNF2 family that localizes to the nucleus and acts at perturbed replication forks and specialized chromatin regions to preserve genome stability. The protein contains an N‑terminal RPA‑binding region, a central helicase ATP‑binding domain and helicase C‑terminal domain, and two HARP (HepA‑related protein) domains that together confer selective binding to forked and RPA‑coated single‑stranded DNA and catalysis of DNA strand re‑annealing, which is the reverse of classical helicase unwinding. SMARCAL1 recognizes stalled replication forks through interaction with replication protein A and fork DNA structures and catalyzes fork regression and restoration, thereby re‑annealing nascent strands and remodeling fork architecture in ways that permit lesion bypass or template switching and protect nascent DNA from degradation during replication stress. The enzyme functions throughout the genome as a DNA translocase that rewinds stably unwound DNA bubbles bound by RPA, acts at stalled forks generated by DNA damage or nucleotide depletion, and contributes to replication fork stability, restart, and completion of DNA synthesis. SMARCAL1 also participates in DNA repair beyond fork remodeling: it acts in double‑strand break responses and telomere maintenance, is phosphorylated by ATM, ATR, and DNA‑PK during DNA damage signaling, and integrates into checkpoint pathways that coordinate replication with repair. In addition to these repair and replication functions, SMARCAL1 binds chromatin and is implicated in chromatin remodeling and transcriptional regulation, with roles described in glucocorticoid‑responsive pathways, pre‑replicative complex activation networks, and, more recently in the regulation of cellular lipid metabolism and innate immune signaling, including suppression of cGAS–STING activation by limiting endogenous DNA damage and modulation of PD‑L1 expression in tumor contexts. Germline loss‑of‑function variants in SMARCAL1 cause Schimke immuno‑osseous dysplasia, an autosomal recessive disorder characterized by spondyloepiphyseal dysplasia, renal dysfunction, T‑cell immunodeficiency, and growth failure, and these alleles disrupt annealing helicase activity or protein production, leading to defective replication stress responses and accumulation of DNA damage in multiple tissues.

Background

SMARCAL1 (SWI/SNF‑related, matrix‑associated, actin‑dependent regulator of chromatin subfamily A‑like 1) is an ATP‑dependent annealing helicase of the SNF2 family that localizes to the nucleus and acts at perturbed replication forks and specialized chromatin regions to preserve genome stability. The protein contains an N‑terminal RPA‑binding region, a central helicase ATP‑binding domain and helicase C‑terminal domain, and two HARP (HepA‑related protein) domains that together confer selective binding to forked and RPA‑coated single‑stranded DNA and catalysis of DNA strand re‑annealing, which is the reverse of classical helicase unwinding. SMARCAL1 recognizes stalled replication forks through interaction with replication protein A and fork DNA structures and catalyzes fork regression and restoration, thereby re‑annealing nascent strands and remodeling fork architecture in ways that permit lesion bypass or template switching and protect nascent DNA from degradation during replication stress. The enzyme functions throughout the genome as a DNA translocase that rewinds stably unwound DNA bubbles bound by RPA, acts at stalled forks generated by DNA damage or nucleotide depletion, and contributes to replication fork stability, restart, and completion of DNA synthesis. SMARCAL1 also participates in DNA repair beyond fork remodeling: it acts in double‑strand break responses and telomere maintenance, is phosphorylated by ATM, ATR, and DNA‑PK during DNA damage signaling, and integrates into checkpoint pathways that coordinate replication with repair. In addition to these repair and replication functions, SMARCAL1 binds chromatin and is implicated in chromatin remodeling and transcriptional regulation, with roles described in glucocorticoid‑responsive pathways, pre‑replicative complex activation networks, and, more recently in the regulation of cellular lipid metabolism and innate immune signaling, including suppression of cGAS–STING activation by limiting endogenous DNA damage and modulation of PD‑L1 expression in tumor contexts. Germline loss‑of‑function variants in SMARCAL1 cause Schimke immuno‑osseous dysplasia, an autosomal recessive disorder characterized by spondyloepiphyseal dysplasia, renal dysfunction, T‑cell immunodeficiency, and growth failure, and these alleles disrupt annealing helicase activity or protein production, leading to defective replication stress responses and accumulation of DNA damage in multiple tissues.

References
https://pubmed.ncbi.nlm.nih.gov/28623093/ pmc.ncbi.nlm.nih.gov/articles/PMC3273839/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%